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Articles by M Shen
Total Records ( 2 ) for M Shen
  A. H Auchincloss , A. V. D Roux , M. S Mujahid , M Shen , A. G Bertoni and M. R. Carnethon
 

Background  Despite increasing interest in the extent to which features of residential environments contribute to incidence of type 2 diabetes mellitus, no multisite prospective studies have investigated this question. We hypothesized that neighborhood resources supporting physical activity and healthy diets are associated with a lower incidence of type 2 diabetes.

Methods  Person-level data came from 3 sites of the Multi-Ethnic Study of Atherosclerosis, a population-based, prospective study of adults aged 45 to 84 years at baseline. Neighborhood data were derived from a population-based residential survey. Type 2 diabetes was defined as a fasting glucose level of 126 mg/dL or higher (≥7 mmol/L) or taking insulin or oral hypoglycemic agents. We estimated the hazard ratio of type 2 diabetes incidence associated with neighborhood (US Census tract) resources.

Results  Among 2285 participants, 233 new type 2 diabetes cases occurred during a median of 5 follow-up years. Better neighborhood resources, determined by a combined score for physical activity and healthy foods, were associated with a 38% lower incidence of type 2 diabetes (hazard ratio corresponding to a difference between the 90th and 10th percentiles for resource distribution, 0.62; 95% confidence interval, 0.43-0.88 adjusted for age, sex, family history of diabetes, race/ethnicity, income, assets, educational level, alcohol use, and smoking status). The association remained statistically significant after further adjustment for individual dietary factors, physical activity level, and body mass index.

Conclusion  Better neighborhood resources were associated with lower incidence of type 2 diabetes, which suggests that improving environmental features may be a viable population-level strategy for addressing this disease.

  H. D Hosgood , C. S Liu , N Rothman , S. J Weinstein , M. R Bonner , M Shen , U Lim , J Virtamo , W. l Cheng , D Albanes and Q. Lan
 

Mitochondria are eukaryotic organelles responsible for energy production. Mitochondrial DNA (mtDNA) lack introns and protective histones, have limited DNA repair capacity and compensate for damage by increasing the number of mtDNA copies. As a consequence, mitochondria are more susceptible to reactive oxygen species, an important determinant of cancer risk, and it is hypothesized that increased mtDNA copy number may be associated with carcinogenesis. We assessed the association of mtDNA copy number and lung cancer risk in 227 prospectively collected cases and 227 matched controls from the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs), adjusting for age at randomization, smoking years and number of cigarettes smoked per day. There was suggestion of a dose-dependent relationship between mtDNA copy number and subsequent risk of lung cancer, with a prominent effect observed in the highest mtDNA copy number quartile [ORs (95% CI) by quartile: 1.0 (reference), 1.3 (0.7–2.5), 1.1 (0.6–2.2) and 2.4 (1.1–5.1); Ptrend = 0.008]. This is the first report, to the best of our knowledge, to suggest that mtDNA copy number may be positively associated with subsequent risk of lung cancer in a prospective cohort study; however, replication is needed in other studies and populations.

 
 
 
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